Indeed, using the new "instability" model of cancer in collaboration with Michael Stratton, PhD, and Andy Futreal, PhD, at the Wellcome Trust Sanger Institute in England, the team discovered a pair of gene mutations involved in a type of human blood cancer.
Stratton, Futreal, Chin, and DePinho are co-senior authors of the report.
As part of the ongoing Cancer Genome Project at the Sanger Institute, its researchers analyzed human cancer cell lines and clinical samples to identify the new mutated genes. These studies have uncovered an unexpectedly large number of genetic alterations present in the typical human cancer genome, presenting challenges in the identification of truly causative events.
DePinho said that the overlap in patterns of genetic abnormalities found in both mouse and human tumors shows that cancer mechanisms in the two species are more alike than had been thought.
Futreal, co-director of the Cancer Genome Project at the Sanger Institute, said that such mouse models and cross-species genomic comparisons will be of "real importance" in facilitating the identification of new human cancer genes and understanding their role in the formation of tumors, "as well as a potential avenue to explore new therapeutic strategies."
Conventional mouse models are made by transferring a cancer-causing oncogene into a mouse embryo. "You plug it into the mouse, and lo and behold, it gets cancer," explained Richard Maser, PhD, of Dana-Farber, one of the studys lead authors. "But that's rigging the game -- it's not identical to the process by which tumors normally arise," he said. These tumors lack some key characteristics of human tumors, such as genomic instability -- pieces of chromosomes breaking apart and reattaching, which result in widespread abnormalities like missing genes or extra copies of genes some of which are essential to the tumors formation.